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At least 19 recordsLinked to original sources
PubMed1992

[Sudden, unexplained infant death--sudden infant death syndrome. Forensic pathological aspects].

Delimitation of the sudden unexplained infant death syndrome (SIDS) is difficult as the diagnosis is made by exclusion. The difficulties in the differential diagnosis are concentrated on interpretation of the significance of positive viral and bacterial findings, inflammatory changes in the respiratory organs, heart and central nervous system together with malformations. Classification of SIDS appears, therefore, to vary according to time and place. New techniques, e.g. DNA analysis, have explained the etiology in a few per cent of the cases but have not yet solved the riddle of SIDS. The article reviews hypotheses about apnoea, arrhythmia, overheating and inefficient surveillance of the infant. It is emphasized that assessment of risk factors for SIDS requires valid epidemiological investigations where the basis for the diagnosis is a uniform classification of SIDS infants as compared with other groups of sudden death in infancy. An investigation of this nature has been initiated in the Nordic countries. It is important to examine and treat infants with abnormal sleep apnoea but generalized employment of monitoring has not reduced the number of unexplained infantile deaths.

Autopsy↗
PubMed1983

[Epidemiology of sudden infant death (sudden infant death syndrome, SIDS) in the Lübeck area. Catamnestic studies of 155 observed cases from 1971 to 1981].

The 155 cases of SIDS investigated at the Institut für Rechtsmedizin of the Medizinische Hochschule in Lübeck (northern part of the Federal Republic of Germany) between 1971 and 1981 have been analysed retrospectively under epidemiological aspects. The incidence was 2.17 cases of SIDS/1,000 live-born babies, 63.9% were male, 79.3% of the infants died during the first 6 months of life with a clear peak in the 2nd month. There was no seasonal accumulation; 68.4% of the infants died between 8.00 p.m. and 8.00 a.m., in 75% the socio-economic factors were inconspicuous, but we observed a significantly higher incidence of infants from mothers younger than 25 years. In 58% of our cases no signs of illness or changed behaviour had been observed during the 48 h before death. The results of our study are compared with the literature and discussed with special regard to a possible prevention.

Age Factors↗
PubMed1994

Absence of ventilatory responses to alternating breaths of mild hypoxia and air in infants who have had bronchopulmonary dysplasia: implications for the risk of sudden infant death.

Infants who have had bronchopulmonary dysplasia (BPD) are at an increased risk of sudden infant death syndrome. Because failure of the cardiorespiratory response to hypoxia is suggested to play a key role in sudden infant death syndrome, we tested the hypothesis that infants who have had BPD have a reduced respiratory chemoreflex response to hypoxia. We examined the reflex respiratory responses to breath-by-breath alternations in fractional inspired oxygen concentration in eight infants who had had BPD (mean gestation = 27 wk, mean postnatal age = 93 d) who were no longer on supplemental oxygen and compared the responses with those of 12 preterm infants who had not required supplemental oxygen or been mechanically ventilated since birth (mean gestation = 30 wk, mean postnatal age = 38 d). For test runs we alternated fractional inspired oxygen concentration through two gas delivery lines between 0.21 and 0.16 on a breath-by-breath basis, and for control runs we alternated the inspirate between the two gas lines with a fractional inspired oxygen concentration of 0.21 in each. Respiration was measured using inductance plethysmography infants with BPD showed no significant differences between test and control responses for any respiratory variable. In contrast, all respiratory variables in the preterm infants showed test responses significantly greater than control. We speculate that the "blunted" chemoreflex respiratory response seen in infants with BPD may predispose them to subsequent respiratory failure, but we do not known which component of the chemoreflex is impaired.

Bronchopulmonary Dysplasia↗
PubMed1996

Tracking strategies involving fourteen sources for locating a transient study sample: parents of sudden infant death syndrome infants and control infants.

Strategies involving 14 sources were used to locate 230 parents of sudden infant death syndrome infants who died in Southern California between 1989 and 1992 and 255 parents of healthy, living infants matched by birth hospital, birth date, race and sex. The sample consisted of adults of reproductive age residing in Southern California. After an event of sudden infant death, many parents moved without a forwarding address; only their names, last known address, and the infant's race, birth date, and sex were available. There was no access to birth certificates, obstetric or pediatric medical records, parents' Social Security numbers, or parents' birth dates. The most successful tracking sources for case parents were the Department of Motor Vehicles, postal service, reverse directory and neighbors, private investigator, and California Medicaid services. For control parents, the post office, Department of Motor Vehicles, and Folks Finders proved the most helpful. Using a combination of the 14 sources achieved an adequate sample size.

Adult↗
PubMed2005

Investigation into sudden infant deaths and unascertained infant deaths in England and Wales, 1995-2003.

This article investigates whether the decline in the sudden infant death rates and the rise in unascertained death rates during the period 1995-2003 were linked. It concludes that changes in certification practices surrounding sudden infant deaths and unascertained deaths suggest that it is becoming more difficult to distinguish between these two causes of death. In addition, there is a huge overlap in the characteristics of babies whose deaths are certified as sudden infant death and those whose death is unascertained. These terms are to some extent used interchangeably. Based on this evidence it seems appropriate to include both groups in any analysis of unexplained infant deaths.

Death Certificates↗
PubMed1988

The relationship between sleep and sudden infant death.

Infants epidemiologically at high risk for SIDS demonstrate a variety of abnormalities in sleep-state organization, maturation, and sleep-state modulation of cardio-respiratory control mechanisms. These involve both the REM and quiet-sleep states and are seen in twins who have had no evidence of clinical cardio-respiratory compromise during infancy as well as in near-miss infants who have suffered serious cardio-respiratory failure. Although these infants have higher levels of REM sleep around 40 weeks, of special concern is the decrease in the maturation of the quiet system, which becomes evident after 44 weeks, and the reported quiet-sleep abnormalities in reflex control of respiration and arousal. The source of these abnormalities is environmental rather than genetic and most likely occurs prenatally. During the critical period for SIDS, infant sleep begins to coalesce from a series of naps to more prolonged night time sleep periods that last up to 8 hours. We believe that the ability to maintain physiologic homeostasis during prolonged sleep is a challenge facing infants who are epidemiologically at risk for sudden infant death. The challenge facing sleep research is the more complete understanding of the relationship between prolonged inhibition, homeostasis, arousal, and development.

Diseases in Twins↗
PubMed2005

[Epidemiology of 25 years of crib death (sudden infant death syndrome) in the Netherlands; incidence of crib death and prevalence of risk factors in 1980-2004].

OBJECTIVE: To describe the prevalence of risk factors and the incidence of cot death (sudden infant death syndrome; SIDS) in the Netherlands during the last 25 years. DESIGN: Descriptive. METHOD: The incidence of cot death/SIDS in infants aged 7-365 days in 1980-2004 was derived from Statistics Netherlands, the Dutch Central Bureau of Statistics. The prevalence of risk factors for cot death/SIDS in the general population was derived from national surveys of baby clinics (0-9 months; 1985-2004) and studies of cot death/SIDS victims (0-23 months; 1984-1991 and 1996/'04). RESULTS: The prevalence of the following risk factors for cot death/SIDS has decreased: primary prone sleeping position (from 60% to 8%), the use of a duvet (from 85% to 18%), maternal smoking (from 34% to 20%), paternal smoking (from 48% to 32%). The prevalence of routine bed-sharing with a parent increased from nearly 0% to 5%. The registered incidence of cot death/SIDS per 100,000 live births decreased from 103 in 1986 to < 15 in 2003 and 2004. The incidence of cot deaths/SIDS that occurred during habitual bed-sharing with a parent, in a playpen, in child-care settings, or in a secondary prone sleeping position increased. CONCLUSION: The incidence of cot death/SIDS and the prevalence of known risk factors for cot death/SIDS has decreased. New risk factors have emerged in recent years. Considering the evolving conditions of infant care, an ongoing study on the special features of child care and the factors involved in cases of cot death/SIDS is warranted. This knowledge is essential for periodic adaptation of the national prevention programme.

Bedding and Linens↗
PubMed1979

The QT interval in aborted sudden infant death syndrome infants.

The QT interval was measured in 12 normal and 7 aborted sudden infant death syndrome (SIDS) infants in rapid eye movement (REM) and quiet sleep at monthly intervals through the age of 4 months. An accuracy of better than 2 msec was assured by high resolution of the digitized signal and calibration of each QT measurement with an accurately generated time code. In contrast to current speculations, the QT index was significantly smaller in the infants with aborted SIDS than in the normal infants in both REM and quiet sleep (P less than 0.05). In addition, as in normal infants, the QTc was smaller in REM than in quiet sleep (P less than 0.01). Although these results offer no support for the hypothesis that SIDS results from prolongation of the QT interval, they suggest that aborted SIDS infants have a functional abnormality in the autonomic nervous system.

Autonomic Nervous System↗
PubMed1981

Attenuated responses to CO2 and hypoxia in parents of threatened sudden infant death syndrome infants.

Ventilatory and heart rate responses to hypercapnia and hypoxia were measured in the following three groups: group I, controls (n equals 15); group II, parents of threatened sudden infant death syndrome (SIDS) infants (n equals 10); and group III, parents of SIDS infants (n equals 17). We found significantly reduced heart rate responses to carbon dioxide and hypoxia in group II (1.4 plus or minus 1.9 percent and 16.0 plus or minus 4.0 percent; mean plus or minus SEM) compared with controls (7.1 plus or minus 1.4 percent and 26 plus or minus 2.4 percent; P less than .025). Ventilatory responses to hypoxia in groups II and III were not significantly different from controls. Two group II mothers had a greatly reduce ventilatory response to carbon dioxide. Four other parents in group II had abnormally low heart rate responses to hypoxia or carbon dioxide. We concluded that parents of threatened SIDS infants had reduced heart rate responses to carbon dioxide and hypoxia and may have reduced ventilatory responses to carbon dioxide.

Adult↗
PubMed1983

Oculocardiac reflex in near miss for sudden infant death syndrome infants.

To gain insight into the role of the vagus nerve in sudden infant death syndrome (SIDS), 180 infants ranging in age from 1 to 66 weeks were examined with respect to cardiac response to ocular compression. There were 35 near-miss infants, 76 normal siblings of SIDS victims, and 69 normal control infants. Asystoles within the control group ranged from 0.3 to 1.8 seconds. Ten of 35 (28%) near-miss infants and 10/76 (13%) siblings had asystoles greater than 2.0 seconds when first tested. When statistically compared, the near-miss infants were significantly different from both the control infants and the siblings (Kruskal-Wallis procedure: P less than .01, and P less than .05, respectively). It is concluded that in the first year of life a significant number of near-miss infants have an exaggerated cardiac response to ocular compression. Furthermore, the presence of prolonged asystoles in certain siblings indicates that vagal hypersensitivity, as manifested by ocular compression, may be, in part, hereditary.

Female↗
PubMed1981

Sleep parameters and respiratory variables in "near miss' sudden infant death syndrome infants.

Twenty-nine near miss for sudden infant death syndrome and thirty normal infants between the ages of 3 weeks and 6 months were monitored polygraphically for 24 hours. The distribution of sleep and abnormal respiratory events were analyzed for both groups. On the basis of mixed and obstructive apnea, 12-hour nocturnal segments (8 PM to 8 AM) consistently distinguished near miss from normal infant groups between the ages of 3 weeks and 4.5 months. Daytime naps do not provide statistical differences sufficient to differentiate between the two groups. During sleep, abnormal respiratory events are more likely to occur between 1 AM and 6 AM, at least 40 minutes after sleep onset. Respiratory pauses show a significant increase just prior to waking (a strong respiratory stimulus). Any impairment of the arousal threshold during sleep will place near miss infants at increased risk.

Monitoring, Physiologic↗